Transcriptomics

Dataset Information

3

Estrogen-driven Prolactin-mediated Gene Expression Networks Hormone Induced Prostatic Dysplasia


ABSTRACT: Emerging evidence suggests that estrogen and prolactin (PRL) play a key role in prostate cancer development, yet their relationship and molecular actions in prostate is not well understood. To address this issue, we made the first direct comparison of estrogen and PRL actions in the Noble rat (NBL) prostate dysplasia model. Prostatic dysplasia in lateral prostate (DLP) has been induced by elevated circulating levels of estrogen and PRL in NBL with estrogen (E2)-filled implants, while physiological level of testosterone (T) was maintained with T-filled implants. The effect of estrogen and PRL was studied by using ICI and bromocriptine (Br) as their respective blockers, both can effectively inhibited dysplasia development under T+E2 induction. Transcript expression profile of the four treatment groups (Control, T+E2, T+E2+Br, and T+E2+ICI) has been characterized in this array.

ORGANISM(S): Rattus norvegicus  

SUBMITTER: Amy N Fullenkamp   Neville C Tam  Shuk-Mei Ho  Johannes M Freudenberg  Mario Medvedovic  Carol Y Szeto 

PROVIDER: E-GEOD-17819 | ArrayExpress | 2010-05-09

SECONDARY ACCESSION(S): GSE17819PRJNA120037

REPOSITORIES: GEO, ArrayExpress

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Publications

Research resource: estrogen-driven prolactin-mediated gene-expression networks in hormone-induced prostatic intraepithelial neoplasia.

Tam Neville N C NN   Szeto Carol Y Y CY   Freudenberg Johannes M JM   Fullenkamp Amy N AN   Medvedovic Mario M   Ho Shuk-Mei SM  

Molecular endocrinology (Baltimore, Md.) 20100922 11


Cotreatment with testosterone (T) and 17β-estradiol (E2) is an established regimen for inducing of prostatic intraepithelial neoplasia (PIN) and prostate cancer in rodent models. We previously used the pure antiestrogen ICI 182,780 (ICI) and bromocriptine, a dopamine receptor agonist, to inhibit PIN induction and systemic hyperprolactinemia in Noble rats and found that the carcinogenic action of T+E2 is mediated directly by the effects of E2 on the prostate and/or indirectly via E2-induced hyper  ...[more]

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